Prevention and Treatment of Mastitis During the Dry Period
The dry (nonlactating) period of the lactation cycle is a critical time for udder health in dairy animals. The major proportion of calf growth occurs during this time, and metabolically this is the most critical time for the cow to prepare for the next lactation.
Prevention of new infections during the dry period hinges on prevention of teat end exposure to environmental pathogens. Rates of new IMI of coliforms are thought to be greater in the dry period than during lactation.58 Thus the same management practices (i.e., maintaining cows in clean, dry, comfortable housing) that prevent infections from these organisms in lactating cows apply to dry cows. The importance of dry cow management is apparent from studies that found that nearly two thirds of clinical coliform mastitis cases in the first 2 months of lactation were newly acquired infections during the dry period.261 The rate of environmental streptococcal IMI was 5.5-fold greater during the dry period as compared to during lactation.261During involution, the mammary gland undergoes marked biochemical, cellular, and immunologic changes. Involution of the mammary parenchyma begins 1 to 2 days after the end of lactation and continues for 10 to 14 days. During this time, the gland is particularly vulnerable to new IMI; in conjunction with the periparturient period, these times represent the greatest risk for new IMI in the lactation cycle of the cow.478 The most important defense, as with lactating cows, remains the teat canal. When a cow is dried off at the end of lactation, the teat canal does not fully fill with keratin for days to months. This contributes to the risk of infection during mammary involution, and cows that have higher milk production at dry-off are more at risk to have teats remain open throughout the dry period.4'9,480 Leukocytes increase to millions per milliliter as involution progresses and then decrease prepartum.
Macrophages are predominate in lacteal secretions, followed by lymphocytes and neutrophils.478 Lactoferrin is also associated with resistance to infection during the nonlactating period.478 Lacteal immunoglobulins increase throughout involution and function by opsonizing bacteria, neutralizing toxins, and preventing bacterial adherence.478 Consequently, the dry period is an ideal time to attain synergy between antibacterial therapy and immune function to eliminate pathogens from the gland and not incur the extensive costs of milk withholding typical of lactating cow therapy.Intramammary administration of antibacterials at the end of lactation (dry cow therapy) has been a standard of dairy mastitis management for 40 years, particularly as a tool to help reduce the prevalence of contagious mastitis. Cure rates for IMI caused by all gram-positive cocci (those IMIs that existed prior to the dry period but were not detected following calving), as with lactational therapy, vary from farm to farm and are dependent on pathogen. A New Zealand study determined that dry cow therapy eliminated 85%, 90%, and 90% of IMIs caused by S. aureus, S. uberis, and S. agalactiae, respectively, as opposed to spontaneous cures of 31%, 50%, and 29% in untreated controls.481,482 Cures for chronic S. aureus IMI or gram-negative organisms may be considerably less.427 However, a ceftiofur dry cow therapy is now labeled for use in North America, and a previous study found that cows that were dry-cow treated with a product with significant activity against gram-negative bacteria (100 mg framycetin, 100 mg penetha- mates, and 300 mg procaine penicillin) had decreased clinical coliform mastitis during the dry period and early lactation as compared to cows treated with cloxacillin.273
Because of concern regarding overuse of antibacterial drugs and potential effects on antimicrobial resistance of bacteria, selective dry cow therapy (treatment of infected cows only) versus total or blanket dry cow therapy (treatment of all cows) is debated.
Although this approach does have the potential to reduce antimicrobial drug use on a dairy farm, it must also be considered how historically successful blanket dry cow therapy has been in both eliminating and preventing IMI during the dry period. Decisions should be carefully made on an individual herd basis, and results should be monitored to determine the success of a dry cow mastitis program based on new IMI during the dry period, probably best monitored by changes in individual cow SCCs, cures of existing infections, and impact on the rate of clinical mastitis, particularly in early lactation. If herds are considering selective dry cow therapy, it is important to consider the ability of the herd to control mastitis (i.e., herds that have BTSCCs >200,000 cells/mL should be advised to reconsider this approach). In addition, not only metrics for outcomes following adoption of selective dry cow therapy should be monitored, but also the criteria for selection of cows that should be either included or excluded for dry cow therapy.140 Herd-specific algorithms should be designed that include at the very least individual cow SCC status before dry-off and clinical mastitis history during the previous lactation, and preferentially bacterial culture status of cows with low SCCs that might be considered to exclude from treatment. Examples of outcomes and various models for selective dry cow therapy have been reported, but the emphasis must be placed on both protocols and outcomes, which will vary greatly depending on the herd.483-485In addition to the role that dry cow therapy has in eliminating existing IMI, one dry cow therapy is also thought to prevent new IMI. Early studies suggested that dry cow therapy reduced new IMI during the dry period by 50%.482 Overall rates from multi-institution studies reported new IMI rates during the dry period as 11% to 25% of quarters in herds that practiced blanket dry cow therapy.486 Intramammary infusion of tilmicosin reduced new infection rates by more than 33% in a Canadian study.486 In addition, selective dry cow therapy can result in more clinical mastitis in the dry period, more new IMI during the dry period, and subsequently more clinical mastitis in early lactation as compared to cows treated with blanket dry cow therapy.487 An internal teat sealant consisting of a bismuth subnitrate paste in a paraffin base has gained wide acceptance on many dairies to create a barrier in the teat canal during the dry period following intramammary infusion.
This is an inert product with no activity or food residue risks. Numerous field studies have confirmed the efficacy of this product to reduce new infection rates over the dry period, especially when used in conjunction with antimicrobial dry cow therapy. As an example, following intramammary cloxacillin at dry-off, the combined use of the teat sealant and antimicrobial infusions resulted in 30% fewer new IMIs during the dry period and 33% fewer clinical mastitis cases from drying off until 60 days in milk, as compared to quarters that were infused with cloxacil- lin only.272As with lactational therapy, the use of systemic administration as an adjunct to intramammary administration has stimulated interest in potential alternative therapeutic regimens. Subcutaneous norfloxacin nicotinate administered at the start of the dry period achieved a better cure rate and lower new infection rate over the dry period for S. aureus infections, as compared to untreated cows and cows administered intramammary cephapirin benzathine preparations.488 However, in a Michigan study, cows administered intramuscular oxytetracycline and intramammary cephapirin did not have better cure rates for quarters infected with S. aureus than cows treated with cep- hapirin only, although this study was performed in a herd that had 50% of the cows infected with S. aureus with a history of long duration of infection.427 Systemic therapy should be reserved for use in dry cows for animals of exceptional value and for infections for which cures are deemed to be difficult to attain (i.e., chronic infections). However, success rates are likely to be low and in most cases will not be worth the injection and withholding time risks, especially if extralabel drugs are administered.
Epidemiology and Management of Mastitis in Heifers
Mastitis in heifers is rarely apparent prior to calving, but few farms actively look for mastitis before parturition. Although many farms raise healthy dairy heifers, in some studies bacteria have been isolated from more than 50% of quarters of prepartum heifers.489-491 Reviews of heifer mastitis studies indicate that the prevalence of mastitis pathogens recovered from mammary secretions obtained before the first parturition ranged from 29% to 74%, whereas the prevalence of infection at first calving ranged from 12% to 57%.227,492 Recovery of Mycoplasma organisms from milk samples was not included in these studies.
Staphylococci (primarily NAS but also S. aureus) are the most frequent isolates recovered from heifers, but environmental pathogens such as streptococci are also frequently recovered.227 NAS are the most common pathogens recovered from heifers and a variety of NAS species have been recovered from teat skin, the streak canal, and precalving udder secretion obtained from heifers.227 While NAS is the most common group of bacteria recovered from postpartum heifers, many of the apparent IMIs spontaneously disappear within the first week after calving. One study indicated that 41% of mammary quarters had NAS infections between days 1 and 4 post calving but 46% of those infections had spontaneously disappeared by days 5 to 8 post calving.493 However, some herds may experience persistent infections with NAS in heifers, resulting in increased SCC values and potentially decreased milk production. These herds require interventions to limit long-term effects on milk quality and production.
Detection of S. aureus in dairy heifers usually indicates that a significant number of lactating cows are infected. Although many herds have controlled S. aureus, regional differences in the prevalence of infected dairy heifers have been reported.492 The exact mechanism of how nonlactating heifers develop S. aureus infections is not known, but studies have demonstrated that teat canals of heifer calves can become colonized at very young ages.494 S. aureus can spread to heifers when they are fed nonpasteurized milk or colostrum or when calves come in contact with objects contaminated with infected milk.495 While ingested milk is not transmitted directly from the digestive tract to the mammary gland, it is possible that calves may lick their udder or legs and colonize the teat skin, eventually leading to increased risk of infection. S. aureus can also be transmitted to heifers during the immediate pre- or postpartum period.
Commingling ill animals and periparturient heifers may result in exposure to infected secretions (milk, blood, feces, etc.) from sick animals. These secretions may remain infectious for variable periods of time (depending on the characteristics of the organism, the type of bedding, and the environmental conditions) and serve as a point of exposure. Milking heifers using equipment that previously has been used on infected cows is also a common route of exposure. Several studies have demonstrated that biting flies can play a role in the transmission of S. aureus between infected and healthy heifers.496 It is thought that flies congregating on teat ends of infected cows can become contaminated with bacteria present in milk droplets and mechanically transfer the bacteria when they land on the teats of uninfected animals.M. bovis is an important pathogen that often affects heifers. This organism is associated with respiratory disease, ear infections, joint infections, mastitis, and other diseases of dairy calves and cows.497 M. bovis dwells primarily in the respiratory tract of cattle, often without causing apparent clinical disease in the host.298 This organism is unique in that respiratory infections can spread through the lymphatic and blood streams to infect other mucosal tissue such as the udder. Animals colonized with M. bovis can develop long-term infections and infect other animals. M. bovis is usually introduced into herds by clinically healthy cattle that are carriers of the organism,497 and bulls have been demonstrated to be carriers.498 M. bovis has been demonstrated to colonize developing udders of prepubertal heifers and eventually cause mastitis.499 The feeding of waste milk from infected cows has long been considered a primary route of infection with M. bovis. Commingling of calves from different sources has consistently been identified as a risk factor for infection with this organism. Control of M. bovis in heifers is based on reducing the potential for contact with potentially infected shedders of the organism and ensuring that calves never receive unpasteurized milk. The organism’s ability to colonize the respiratory tract of cattle also requires strict attention to limiting the potential for airborne transmission, thus adequate ventilation, isolation of calves from older animals or ill calves, and reduced stocking densities are commonsense precautions.
RISK FACTORS FOR MASTITIS IN HEIFERS. Most risk factors that contribute to the development of mastitis in heifers are related to exposure of heifers to mastitis-causing organisms. The exception to this is the occurrence of udder edema. Calves that are group-housed have the opportunity for cross-suckling, leading to increased risk for transmission of contagious pathogens.500 Several studies have shown that contact of heifers with older cows before calving (even housing in the same barn) increases the risk of clinical mastitis after calving, and separation of heifers from older cows is generally recommended.501 The hygiene of the environment is also an important determinant of the risk of developing mastitis in heifers, and this is true for heifers raised on pasture as well as heifers raised in confinement.502
PREVENTION OF MASTITIS IN HEIFERS. Prevention of mastitis in heifers is based on reducing exposure to mastitis pathogens and enhancing the ability of the heifers’ immune system to respond to exposure. Prevention of mastitis in heifers includes the following strategies: (1) Controlling the prevalence of mastitis in the existing adult herd—exposure to contagious mastitis is more likely to occur when many animals are infected as compared to when few animals are infected; (2) using individual stalls for preweaned calves; (3) culling calves that persist in suckling other calves; (4) feeding milk replacer or pasteurized milk from healthy, uninfected cows rather than waste milk; (5) controlling flies—especially important in the control of S. aureus; (6) milking fresh heifers first using clean milking equipment; (7) calving heifers in clean pens that have not been used to house sick cows; (8) housing growing and prepartum heifers in an adequately bedded area that is clean and dry and provides sufficient space for all animals; (9) feeding a well-balanced diet that enhances the immune systems of the heifers—recommended values include 1000 IU per day vitamin E during the prefresh period and adequate selenium; (10) boosting the immunity of heifers by using gram-negative J5 vaccines, which work to reduce the severity of infections caused by gram-negative bacteria such as E. coli; and (11) considering prepartum teat dipping several times a week for problem herds503 or the use of internal teat sealants administered about 1 month before calving.504
PREPARTUM TREATMENT OF HEIFERS. Intramammary therapy with antibiotics is one of the tools used to control mastitis in heifers.494 Intramammary treatment of prepartum heifers is generally considered efficacious in reducing the prevalence of infection, can result in a reduction of SCC, and in some cases has been shown to increase milk production in the subsequent lactation.496,505-508 However, research shows that the production response is highly variable among herds and this strategy should be routinely recommended only for herds that have demonstrated problems with heifer mastitis.509 Oliver and colleagues510 reported cure rates of 84% and 97%, respectively, for heifers infected with NAS that received intramammary treatment using 200 mg of either sodiumcloxacillin or cephapirin sodium; the spontaneous cure rate was 27% for heifers in an untreated control group. Research has shown that administration of intramammary antimicrobial treatments during late gestation is generally highly effective and cure rates for staphylococcal infections frequently exceed 90%.510 Intramammary products designed for both lactating and nonlactating cows (dry cow products) have been evaluated for use in precalving heifers.494 In virtually all instances, high rates of bacteriologic cure have been reported. No significant difference in treatment efficacy was found based on treatments given during the first, second, or third trimester of pregnancy, but fewer new S. aureus infections were reported for animals treated in the third trimester.506,511 However, to minimize the potential for residues after calving, treatments should be administered at least 60 days before the expected due date, and milk should be checked for residues after calving. Unlike intramammary treatments, systemic antibiotics administered to heifers have not been shown to be effective in reducing the incidence of mastitis.512 The effect of precalving treatment on production of heifers appears to be variable among herds and is not performed without introducing the risk of infections caused by improper administration of the intramammary tubes. The administration of internal teat sealants or intramammary antibiotics should occur only under hygienic conditions and after effective sanitation of teat ends. This practice is generally recommended only for herds that have demonstrated problems with mastitis in heifers.